Pepsin Activity In Gastric Juice Research Articles

Novel approach to gastric mucosal defect repair using fresh amniotic membrane allograft in dogs (experimental study)

BackgroundGastric mucosal defect could result from several causative factors including the use of nonsteroidal anti-inflammatory drugs, Helicobacter pylori infection, gastrointestinal and spinal cord diseases, and neoplasia. This study was performed to achieve a novel simple, inexpensive, and effective surgical technique for the repair of gastric mucosal defect.MethodsSix adult male mongrel dogs were divided into two groups (three dogs each). In the control positive group (C + ve), dogs were subjected to surgical induction of gastric mucosal defect and then treated using traditional medicinal treatment for such a condition. In the amniotic membrane (AM) group, dogs were subjected to the same operation and then fresh AM allograft was applied. Clinical, endoscopic, biochemical (serum protein and lipid and pepsin activity in gastric juice), histopathological, and immunohistochemistry evaluations were performed.ResultsRegarding endoscopic examination, there was no sign of inflammatory reaction around the grafted area in the AM group compared to the C + ve group. The leukocytic infiltration in the gastric ulcer was well detected in the control group and was less observed in the AM group. In the AM group, the concentrations of both protein and lipid profiles were nearly the same as those in serum samples taken preoperatively at zero time, which indicated that the AM grafting acted the same as gastric mucosa. The re-epithelization of the gastric ulcer in the C + ve group was not yet detected at 21 days, while in the AM group it was well observed covering most of the gastric ulcer. AM accelerated the re-epithelization of the gastric ulcer. The fibrous connective tissue and the precursor of collagen (COL IA1) were poorly detected in the gastric ulcer with AM application.ConclusionUsing fresh AM allograft for repairing gastric mucosal defect in dogs showed great impact as a novel method to achieve optimum reconstruction of the gastric mucosal architecture and restoration of pre-epithelial, epithelial, and post-epithelial normal gastric mucosal barriers.

Protective effect of hydrogen sulfide against cold restraint stress-induced gastric mucosal injury in rats

Hydrogen sulfide (H2S) is an endogenous gaseous mediator plays a potential role in modulating gastric inflammatory responses. However, its putative protective role remains to be defined. The present study aimed to evaluate role of the exogenously released and endogenously synthesized H2S in cold restraint stress (CRS)-induced oxidative gastric damage in rats. Rats were restrained, and maintained at 4°C for 3h. The H2S donor, sodium hydrosulfide (NaHS) (60μmol/kg) was injected intraperitoneally (i.p.) before CRS. Our results revealed that NaHS pretreatment significantly attenuated ulcer index, free and total acid output, and pepsin activity in gastric juice along with decreased gastric mucosal carbonyl content and reactive oxygen species production. This was accompanied by increased gastric juice pH and mucin concentration in addition to restoring the deficits in the gastric reduced glutathione, catalase as well as superoxide dismutase enzyme activities. NaHS pretreatment markedly reduced the serum level of tumor necrosis factor (TNF-α) and myeloperoxidase activity compared to CRS-non-treated. Moreover, NaHS preadministration significantly abrogated the inflammatory and the deleterious responses of gastric mucosa in CRS. The protective effects of H2S were confirmed by gastric histopathological examination. However, pretreatment with the H2S-synthesizing enzyme, cystathionine-gamma-lyase inhibitor, beta-cyano-L-alanine (50mg/kg, i.p.) reversed the gastroprotection afforded by the endogenous H2S. Collectively, our results suggest that H2S can protect rat gastric mucosa against CRS-induced gastric ulceration possibly through mechanisms that involve anti-oxidant and anti-inflammatory actions alongside enhancement of gastric mucosal barrier and reduction in acid secretory parameters.

Mechanisms of the Protective Effects of Curcumin against Indomethacin-Induced Gastric Ulcer in Rats

Background/Aims: Curcumin, a naturally occurring polyphenolic compound, exhibits anti-inflammatory and antioxidant properties that render it an attractive candidate for protection against gastric ulcer. The aim of this study is therefore to evaluate the protective effects of curcumin against indomethacin-induced gastric ulcer in rats. Methods: Gastric ulceration was induced by a single intraperitoneal injection of indomethacin (30 mg/kg). Curcumin (50 mg/kg, p.o.) was administered 30 min before ulcer induction. Results: Curcumin showed gastroprotective effects as evidenced by significant decreases in ulcer index, total acid output and pepsin activity in gastric juice in addition to gastric mucosal malondialdehyde concentration, and concomitant increases in gastric juice mucin concentration, gastric mucosal nitric oxide level and catalase and superoxide dismutase activities as compared to the indomethacin-induced ulcer group. Moreover, immunohistochemical investigations demonstrated that curcumin treatment markedly decreased expression of inducible nitric oxide synthase, nuclear factor-κB, and caspase-3. Conclusion: Curcumin protected the rats' gastric mucosa against indomethacin-induced gastric ulceration possibly, at least in part, by enhancement of the gastric mucosal barrier and reduction in acid secretory parameters in addition to antioxidant and antiapoptotic activities.

Protective effects of nebivolol against cold restraint stress-induced gastric ulcer in rats: Role of NO, HO-1, and COX-1,2

Nebivolol, a β1-adrenoceptor antagonist, exhibits vasodilatory and anti-oxidative properties that rendering it attractive candidate for protecting against gastric ulcer. The aim of this study therefore is to evaluate the protective effects of nebivolol against cold restraint stress (CRS)-induced gastric ulcer in rats. Rats were restrained, and maintained at 4°C for 3h. Nebivolol (5mg/kg, p.o.) was suspended in 0.5% aqueous solution of carboxymethyl cellulose and was administered 30min before CRS. Nebivolol exhibited gastroprotective effects as evidenced by significant decreases in ulcer index as well as free and total acid output, and pepsin activity in gastric juice in addition to gastric mucosal malondialdehyde concentration, with concomitant increases in gastric juice pH and mucin concentration along with gastric mucosal reduced glutathione and nitric oxide (NO) concentrations compared with CRS rats. Moreover, immunohistochemical analysis demonstrated that nebivolol treatment markedly enhanced heme oxygenase-1 as well as cyclooxygenase-1 and cyclooxygenase-2 expressions. The protective effects of nebivolol were confirmed by gastric histopathological examination. Pretreatment with Nω-nitro-l-arginine, a NO synthase inhibitor, partly altered the protection afforded by nebivolol. In conclusion, nebivolol protected rats’ gastric mucosa against CRS-induced gastric ulceration possibly through anti-oxidant activity, enhancement of gastric mucosal barrier and reduction in acid secretory parameters.

Mucosal protective effects of ecabet sodium: pepsin inhibition and interaction with mucus

Pepsin, acid and Helicobacter pylori are major factors in the pathophysiology of peptic ulcer disease and reflux oesophagitis. Ecabet sodium reduces the survival of H. pylori in the stomach and inhibits pepsin activity in the gastric juice of experimental animals. Here we have investigated the effects of ecabet sodium on some of the factors involved in the dynamics of the mucosal barrier, i.e. pepsins and mucins. This study used gastric juice obtained from 12 non-symptomatic volunteers and nine patients with reflux oesophagitis. Ecabet sodium significantly inhibited pepsin activity in human gastric juice, with a maximum inhibition of 78%. Pepsin 1, the ulcer-associated pepsin, was inhibited to the greatest extent. The ability of gastric juice to digest mucin was significantly inhibited by ecabet. As with gastric juice proteolytic activity, the inhibitory effect of ecabet on mucolysis was greater in gastric juice from patients with reflux oesophagitis than in that from controls. Ecabet sodium showed a positive interaction with gastric mucin, as assessed by an increase in viscosity. Thus ecabet sodium may reduce the aggressive potential of gastric juice towards the mucosa, which may be relevant in the treatment of reflux oesophagitis and peptic ulcer disease. In addition, it may strengthen the mucus barrier in peptic ulcer disease and gastritis.

Mucosal protective effects of ecabet sodium: pepsin inhibition and interaction with mucus

Pepsin, acid and Helicobacter pylori are major factors in the pathophysiology of peptic ulcer disease and reflux oesophagitis. Ecabet sodium reduces the survival of H. pylori in the stomach and inhibits pepsin activity in the gastric juice of experimental animals. Here we have investigated the effects of ecabet sodium on some of the factors involved in the dynamics of the mucosal barrier, i.e. pepsins and mucins. This study used gastric juice obtained from 12 non-symptomatic volunteers and nine patients with reflux oesophagitis. Ecabet sodium significantly inhibited pepsin activity in human gastric juice, with a maximum inhibition of 78%. Pepsin 1, the ulcer-associated pepsin, was inhibited to the greatest extent. The ability of gastric juice to digest mucin was significantly inhibited by ecabet. As with gastric juice proteolytic activity, the inhibitory effect of ecabet on mucolysis was greater in gastric juice from patients with reflux oesophagitis than in that from controls. Ecabet sodium showed a positive interaction with gastric mucin, as assessed by an increase in viscosity. Thus ecabet sodium may reduce the aggressive potential of gastric juice towards the mucosa, which may be relevant in the treatment of reflux oesophagitis and peptic ulcer disease. In addition, it may strengthen the mucus barrier in peptic ulcer disease and gastritis.

Total pepsin activity in gastric juice in prepyloric gastric ulcer (PPGU) and in duodenal ulcer (DU): Helicobacter pylori (HP) influence

Total pepsin activity in gastric juice in prepyloric gastric ulcer (PPGU) and in duodenal ulcer (DU): Helicobacter pylori (HP) influence

Influence of Lansoprazole on Intragastric 24-Hour pH, Meal-Stimulated Gastric Acid Secretion, and Concentrations of Gastrointestinal Hormones and Enzymes in Serum and Gastric Juice in Healthy Volunteers

Twelve healthy volunteers (6 females, 6 males) between 26 and 36 years of age were enroled in this double-blind, randomized, placebo-controlled, three-way cross-over study. The objective was to determine the influence of lansoprazole (Agopton, Takeda Pharma GmbH, Aachen), a novel proton pump inhibitor, in doses of 30 and 60 mg, on the intragastric pH, on meal-stimulated gastric acid secretion and on the concentration of gastrointestinal hormones and enzymes in serum and gastric juice. Active drug or placebo had to be taken as single daily morning doses on an empty stomach for 7 days. Each wash-out period between drug application periods was 2 weeks long. Lansoprazole induced a dose-related increase in intragastric pH as well as a relevant reduction of basal acid output, meal-stimulated acid output and meal-stimulated secretion volume. 60 mg lansoprazole was significantly superior to 30 mg in increasing intragastric pH. The basal secretion volume in volunteers on 30 and 60 mg lansoprazole were lower than in volunteers on placebo. Serum gastrin and serum pepsinogen concentrations increased in a dose-dependent manner. Pepsin output and pepsin activity in gastric juice were slightly decreased in volunteers on 30 mg lansoprazole and markedly suppressed in volunteers on 60 mg lansoprazole 2 h after meal stimulation. Intrinsic factor concentration increased in volunteers on lansoprazole with a clear dose relationship. The evaluation of laboratory data and reported nonserious adverse events proved the relative safety of this new antiulcer agent.

A semi-automated method for the determination of pepsin activity in gastric juice using the Tecan liquid-handling system

Conference Article| February 01 1988 A semi-automated method for the determination of pepsin activity in gastric juice using the Tecan liquid-handling system ANDREW G. LYNN; ANDREW G. LYNN *Departments of Biochemistry, Pharmacology; Reckitt and Colman plc, Pharmaceutical Division, Dansom Lane, Hull, North Humberside HU8 7DS, U.K. Search for other works by this author on: This Site PubMed Google Scholar ANTHONY C. LANE; ANTHONY C. LANE *Departments of Biochemistry, Pharmacology; Reckitt and Colman plc, Pharmaceutical Division, Dansom Lane, Hull, North Humberside HU8 7DS, U.K. Search for other works by this author on: This Site PubMed Google Scholar LYNDA A. SMEATON LYNDA A. SMEATON †Pharmacology; Reckitt and Colman plc, Pharmaceutical Division, Dansom Lane, Hull, North Humberside HU8 7DS, U.K. Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (1988) 16 (1): 26–27. https://doi.org/10.1042/bst0160026 Article history Received: June 15 1987 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation ANDREW G. LYNN, ANTHONY C. LANE, LYNDA A. SMEATON; A semi-automated method for the determination of pepsin activity in gastric juice using the Tecan liquid-handling system. Biochem Soc Trans 1 February 1988; 16 (1): 26–27. doi: https://doi.org/10.1042/bst0160026 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search This content is only available as a PDF. © 1988 Biochemical Society1988 Article PDF first page preview Close Modal You do not currently have access to this content.

Antipeptic activity of a sulfate glycopeptide different behavior with purified human pepsin or human gastric juice.

A sulfated glycopeptide with antiulcer properties in animals and man was administered orally to 10 patients with duodenal ulcer, and its effects on peptic activity tested in vivo. A synthetic dipeptide,N-acetyl-l-phenylalanyl-l-diiodotyrosine, was used as substrate. Sulfated glycopeptide, 50 and 100 mg, completely inhibited peptic activity 15 minutes after administration in 2 of 3 patients and 3 of 3 patients examined, respectively; the inhibitory effect lasted 30 minutes. Sulfated glycopeptide, 200 mg, completely inhibited peptic activity in 4 of 4 patients examined 15 minutes after administration. In 2 patients complete enzymatic inhibition lasted 1 hour. In vitro, sulfated glycopeptide inhibited peptic activity of human gastric juice but not of purified human pepsin. These results may indicate that pepsin is present in gastric juice as a component of a mucoprotein complex. Sulfated glycopeptide may inhibit pepsin activity in gastric juice by directly precipitating this glycoproteic complex.

Studies on oxidized starch sulfates for medical purposes. IV. Protective effect of sulfates of oxidized starch and its reduced products on experimental peptic ulceration.

Sulfates of oxidized starch and its reduced products were investigated for their protective effect on experimental peptic ulceration. 1) Both oxidized starch sulfate and sulfate of reduced product of oxidized starch with various sulfur content and viscosity showed protective effect on ulceration of Shay rats when administered in 30 mg. doses intra-esophageally, and the protective effect is enhanced with increasing sulfur content, just the same as their inhibitory activity on proteolytic action in vitro. 2) Their protective effect on ulceration is closely related to the loss of pepsin activity in gastric juice. The decrease in pepsin activity is proportional to the decrease in ulceration rate. From the fact that they had no protective effect on ulceration by subcutaneous administration, their protective effect may be caused by their direct inhibition of pepsin activity in gastric juice. 3) They had no protective effect on Takagi's stress rats by intra-esophageal administration.